Abstract: TH-PO1135
Sorafenib Induced Resistant Hypocalcemia in a Patient with Chronic Mild Hypocalcemia from Possible Lysozyme Induced Nephropathy: A Nightmare to Treat
Session Information
- Fluid, Electrolyte, Acid-Base Disorders
November 02, 2017 | Location: Hall H, Morial Convention Center
Abstract Time: 10:00 AM - 10:00 AM
Category: Fluid, Electrolytes, and Acid-Base
- 704 Fluid, Electrolyte, Acid-Base Disorders
Authors
- Gupta, Sanjeev, Westchester Medical Center, Valhalla, New York, United States
- Papanagnou, Anastasios, Westchester Medical Center, Valhalla, New York, United States
- Al Azzi, Yorg, Westchester Medical Center, Valhalla, New York, United States
- Brogan, Maureen E., Westchester Medical Center, Valhalla, New York, United States
Background
Sorafenib is a multikinase inhibitor; approved for treatment of multiple cancers. A lesser-known side effect of this drug is hypocalcemia (hypoCa). Diarrhea and Vit D malabsorption due to exocrine pancreatic dysfunction are proposed causes for hypoCa from Sorafenib. We present a case of Sorafenib induced severe hypoCa in a patient with chronic mild asymptomatic hypoCa.
Methods
A 67-year-old man with a history of CMML, MDS and hypoCa with c/o joint pain and weakness admitted for management of possible AML. Work-up showed anemia, thrombocytopenia, and leukocytosis. Bone marrow aspiration confirmed AML. A single dose of Cytarabine and Sorafenib was administered. His serum calcium (S.Ca) dropped to 6.2 from 7.9 (at admission). IV and oral calcium with Vit D were initiated. The patient, however, became symptomatic with oral numbness due to a further drop in S.Ca to 5.8. IV calcium drip was added to oral calcium and Vit D. His S.Ca was difficult to maintain above 7, even on an IV calcium drip with Vit D. High-dose IV calcitriol was added to the treatment plan. His PTH and 25-Vit D levels were 576 and 20 respectively. Given his history of CMML, lysozyme-induced proximal RTA was considered as an underlying etiology of chronic hypoCa supported by glycosuria, high fractional excretion of phosphate, elevated trans-tubular potassium gradient and increased urinary level of alpha-aminobutyric acid, alanine, arginine, and asparagine. His urinary Ca/Cr ratio was low (<7). The patient finally responded to treatment and was subsequently switched to oral calcium and calcitriol and discharged home with S.Ca of 7.9.
Conclusion
Lysozyme-induced nephropathy is an under-recognized complication of CMML. A persistently elevated level of lysozyme exceeds the reabsorption capacity of tubules leading to tubular injury. The exact mechanism of action of Sorafenib induced hypoCa is still unknown attributing to challenges in managing such patients. Our patient’s S.Ca level did not respond well to Vit D as suggested by few case reports and required heavy doses of calcitriol along with IV calcium and Vit D analogues. This case highlights that it is essential to consider underlying history of hypoCa before starting a patient on Sorafenib, as it can lead to severe hypoCa, which can be difficult to manage.